A drug currently used to treat osteoporosis has shown promise in blocking spinal damage in a recent study. The research, conducted using zebrafish, found that altered gene activity can lead to mineral accumulation in the spine. This process hardens spinal tissue and resembles bone formation in unintended areas.
Researchers observed that zebrafish bred with a faulty collagen-related gene developed spinal abnormalities. These included fused vertebrae and mineral deposits that made the tissue between bones abnormally hard. This condition closely mirrored intervertebral disc degeneration (IVDD) in humans.
The study identified that the mineralization did not occur immediately. It followed the deterioration of a supportive scaffold layer within the developing spine. Analysis of gene activity in the fish revealed issues with fat processing, the mTOR pathway regulating growth, phosphate control, and vitamin A signaling. These processes are all linked to abnormal mineral accumulation.
Several methods reduced the spinal damage in the zebrafish. A bisphosphonate, an osteoporosis medication, prevented mineral buildup. Reducing food intake or administering drugs that suppressed fat metabolism also decreased spinal fusion. These findings suggest that phosphate regulation and fat metabolism are promising targets for new treatments.
Intervertebral disc degeneration is a major cause of back pain. No medications currently exist to stop or reverse its progression. This discovery points to potential new therapeutic approaches beyond surgical intervention. The study was funded by Arthritis UK and BBSRC and published in *Communications Biology*.
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